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VIP Neuroinflammation: Research Application Comparison
| Disease Model | VIP Mechanism Targeted | Outcome Measure | Improvement vs Control | Administration Route | Study Duration | Professional Assessment ||—|—|—|—|—|—|| Experimental Autoimmune Encephalomyelitis (EAE / MS model) | VPAC1-mediated NF-κB inhibition i
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- | Disease Model | VIP Mechanism Targeted | Outcome Measure | Improvement vs Control | Administration Route | Study Duration | Professional Assessment ||—|—|—|—|—|—|| Experimental Autoimmune Encephalomyelitis (EAE / MS model) | VPAC1-mediated NF-κB inhibition in microglia and T-cells | Clinical disease score, CNS demyelination area | 45–62% reduction in peak disease severity, 38% reduction in demyelination | Intraperitoneal (IP) or intranasal | 21–35 days | VIP shows consistent efficacy across multiple EAE protocols. Most robust data exists for relapsing-remitting models, less clear benefit in progressive phenotypes || Middle Cerebral Artery Occlusion (stroke) | Microglial M2 polarization, reduced MMP activity at BBB | Infarct volume, neurological deficit score | 32–41% reduction in infarct volume, 28% improvement in motor function at 14 days | Intranasal or IV bolus within 3h of reperfusion | 14–28 days | Time-sensitive intervention. Efficacy drops sharply if administered >6 hours post